scholarly journals Clonal structure of invasiveStreptococcus pyogenesin Northern Scotland

1995 ◽  
Vol 115 (2) ◽  
pp. 231-241 ◽  
Author(s):  
M. Upton ◽  
P. E. Carter ◽  
M. Morgana ◽  
G. F. Edwards ◽  
T. H. Pennington
Keyword(s):  
Severe Infection ◽  
Restriction Endonuclease Analysis ◽  
Molecular Techniques ◽  
Clonal Structure ◽  
The Usa ◽  
Group A ◽  
Polymerase Chain ◽  
Serious Disease ◽  
Type 3

SummaryWe have used molecular techniques to characterize 51 group A streptococci from Scotland and 17 ‘serious disease’ isolates from other countries, in order to establish the clonal structure of invasiveStreptococcus pyogenesstrains circulating between 1986 and 1993. Strains were grouped by restriction endonuclease analysis, pulsed field gel electrophoresis and ribotyping patterns, and were examined for the presence of alleles of thespeAgene by polymerase chain reaction and DNA sequence analysis. Serious and fatal infections in Scotland were caused by several clones. One clone (9 of 51 strains) was M type 1 and possessed thespeAgene allele 2. This was the clone previously identified as causing severe infection in the USA. Another clone (5 of 51 strains) was M type 3 and hadspeAgene allele 3. In view of the clear association of more than one clone with severe, invasive and fatal infections, horizontal gene exchange between genotypes merits further investigation.

scholarly journals M Type 1 and 3 Group A Streptococci Stimulate Tissue Factor-Mediated Procoagulant Activity in Human Monocytes and Endothelial Cells

2003 ◽  
Vol 71 (4) ◽  
pp. 1903-1910 ◽  
Author(s):  
A. E. Bryant ◽  
S. M. Hayes-Schroer ◽  
D. L. Stevens
Keyword(s):  
Endothelial Cells ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Tissue Factor ◽  
Multiple Organ ◽  
Group A Streptococci ◽  
Human Monocytes ◽  
Group A ◽  
Type 3

ABSTRACT Streptococcal toxic shock syndrome (StrepTSS) is an invasive infection characterized by marked coagulopathy, multiple organ failure, and rapid tissue destruction and is strongly associated with M type 1 and 3 group A streptococci (GAS). Initiation of the coagulation cascade with formation of microvascular thrombi contributes to multiple organ failure in human cases of gram-negative bacteremia; however, little is known regarding the mechanism of coagulopathy in StrepTSS. Thus, we investigated the abilities of several strains of M type 1 and 3 GAS isolated from human cases of StrepTSS to stimulate production of tissue factor (TF), the principal initiator of coagulation in vivo. Washed, killed M type 1 and 3 GAS, but not M type 6 GAS, elicited high-level TF-mediated procoagulant activity from both isolated human monocytes and cultured human umbilical vein endothelial cells. M type 1 GAS consistently elicited higher levels of TF from monocytes than did M type 3 GAS. GAS-induced TF synthesis in monocytes did not correlate with production of tumor necrosis factor alpha or interleukin-8. Conversely, M type 3 GAS were consistently more potent than M type 1 GAS in stimulating endothelial cell TF synthesis. These results demonstrate that (i) M type 1 and 3 strains of GAS are potent inducers of TF synthesis, (ii) GAS-induced TF synthesis is not simply an epiphenomenon of cytokine generation, and (iii) induction of TF in endothelial cells and monocytes may be M type specific. In total, these findings suggest that a novel interaction between GAS and host cells contributes to the observed coagulopathy in StrepTSS.

scholarly journals THE SIGNIFICANCE OF M AND T ANTIGENS IN THE CROSS REACTIONS BETWEEN CERTAIN TYPES OF GROUP A HEMOLYTIC STREPTOCOCCI

1940 ◽  
Vol 71 (4) ◽  
pp. 539-550 ◽  
Author(s):  
Rebecca C. Lancefield
Keyword(s):  
Specific Antigen ◽  
Specific Protein ◽  
T Antigens ◽  
Cross Reactions ◽  
Group A ◽  
Specific Antigens ◽  
The Cross ◽  
Type 3

In any one strain the occurrence of the previously recognized type-specific protein, M, is usually completely correlated with the presence of the recently recognized type-specific antigen, T. Strain C203 is exceptional in having the T substance of type 1 as well as the two type-specific antigens, M and T, characteristic of type 3. It does not have the M antigen of type 1. While other strains with similar antigenic peculiarities have not been encountered, it is probable that they occur, and the existence of such anomalies must be suspected when unusual serological reactions occur.

scholarly journals Swept-Source Optical Coherence Tomography Angiography According to the Type of Choroidal Neovascularization

2019 ◽  
Vol 8 (9) ◽  
pp. 1272 ◽  
Author(s):  
Joon Hyung Yeo ◽  
Hum Chung ◽  
Jee Taek Kim
Keyword(s):  
Optical Coherence Tomography ◽  
Demographic Characteristics ◽  
Neovascular Amd ◽  
Swept Source ◽  
Group A ◽  
Group B ◽  
Type 3 ◽  
Cnv Detection

We analyzed and compared the sensitivity of choroidal neovascularization (CNV) detection according to CNV type in patients with active neovascular age-related macular degeneration (AMD) using swept-source optical coherence tomography (OCT) angiography (OCTA). A retrospective chart review was performed in patients with neovascular AMD. OCTA images were classified into three groups: Group A (well-circumscribed vascular complex); Group B (moderately circumscribed vascular complex); and Group C (poorly circumscribed vascular complex), according to CNV appearance. Demographic characteristics, OCT parameters, neovascularization subtypes, and OCTA image quality were analyzed to determine the effect on visualization of the neovascular complex. A total of 130 patients with CNV secondary to active neovascular AMD were analyzed. Among them, 52 eyes from 47 patients were included in the study. Eighteen eyes (34.6%) were classified into Group A, 24 (46.2%) into Group B, and 10 (19.2%) into Group C. Statistical analysis showed no significant differences in demographic characteristics or OCT parameters between the three groups. Overall sensitivity of active CNV detection was 80.7% (42/52 eyes). In 73.5% (25/34) of eyes with type 1 CNV (sub-retinal pigment epithelial type), 100.0% (9/9) of eyes with type 2 CNV (sub-retinal type), and 88.9% (8/9) of eyes with type 3 CNV (retinal angiomatous proliferation type), the vascular complex was well visualized on OCTA. OCTA provides adequate noninvasive imaging of CNV in patients with neovascular AMD, which may assist in CNV diagnosis and activity monitoring. In particular, type 2 CNV was well detected in OCTA in comparison with type 1 and type 3 CNV.

scholarly journals Current Epidemiology of Serogroup W Meningococcal Disease—United States, 2010–2015

2017 ◽  
Vol 4 (suppl_1) ◽  
pp. S7-S7 ◽  
Author(s):  
Heidi Soeters ◽  
Amy Blain ◽  
How-Yi Chang ◽  
Melissa Whaley ◽  
Jessica Macneil
Keyword(s):  
New York ◽  
Meningococcal Disease ◽  
Clonal Complex ◽  
Case Fatality ◽  
Severe Infection ◽  
Stable Range ◽  
Disease Epidemiology ◽  
The Usa ◽  
Polymerase Chain ◽  
The Uk

Abstract Background Serogroup W (NmW) meningococcal disease is a rare but severe infection. Following an NmW outbreak after the Hajj in 2000, NmW disease, predominantly caused by sequence type (ST)-11 clonal complex (cc), rapidly increased in South Africa, South America, and the UK. We describe NmW meningococcal disease epidemiology in the USA during 2010–2015. Methods Data were collected from the National Notifiable Diseases Surveillance System, Active Bacterial Core surveillance, and state health departments. Isolates were serogrouped via slide agglutination and real-time polymerase chain reaction. For cases lacking a serogroup result at CDC, the state result was used. Case-fatality ratios (CFR) were calculated using the proportion of cases with known outcomes as the denominator. cc and ST were determined using multilocus sequence typing (MLST). Results From 2010 to 2015, 3,504 meningococcal disease cases were reported to CDC; 2,976 (85%) had a serogroup result, of which 290 (10%) were NmW. Although the number of NmW cases reported annually remained fairly stable (range: 40–57), the total number of reported meningococcal disease cases decreased by 60%, and the proportion of cases due to NmW increased from 6% (42/830) in 2010 to 12% (40/332) in 2015. The majority of NmW cases were reported from five states: Florida (n = 106), California (n = 31), New York (n = 25), Georgia (n = 19), and Oregon (n = 11). Half of people with NmW disease were male, 185 (64%) were white, and 84 (29%) were Hispanic. The median age was 51 years (interquartile range: 26–70). Overall, 20% (52/259) of NmW cases were fatal, compared with CFRs for serogroups B (15%), Y (18%), or C (24%). NmW CFR was highest among adults aged 50–59 years (38%). MLST results were available for 119 (41%) of NmW cases: 76 (64%) were cc11, 40 (34%) were cc22, and 1 each were cc23, cc32, and an unassigned cc. cc appeared to be geographically associated: cc11 was concentrated in Florida and Georgia, while cc22 predominated on the West coast. Within cc11, the majority of isolates (86%) were ST-11, and within cc22 the majority (73%) were ST-22. Conclusion A rapid increase in NmW disease has not been observed in the USA. Most NmW cases were reported in a limited number of states, with geographic differences in clonal complex. Disclosures All authors: No reported disclosures.

scholarly journals A humán parechovírusok klinikai jelentősége súlyos újszülött- és csecsemőkori fertőzésekben hazánkban

2019 ◽  
Vol 160 (10) ◽  
pp. 386-395
Author(s):  
Ákos Boros ◽  
Zsófia Hamarics ◽  
Hajnalka Fenyvesi ◽  
Zoltán Liptai ◽  
Zoltán Nyul ◽  
...  
Keyword(s):  
Clinical Symptoms ◽  
Neurological Symptoms ◽  
Human Parechovirus ◽  
Faecal Samples ◽  
Group A ◽  
Polymerase Chain ◽  
Group B ◽  
Loss Of Appetite ◽  
Leading Symptom

Abstract: Introduction: Most human parechovirus (HPeV, family Picornaviridae) infections are asymptomatic but may cause gastroenteritis in children. New reports show that HPeVs can be associated with severe central nervous system symptoms and sepsis-like syndromes in infants. The clinical significance of HPeVs in Hungary has not been investigated before. Aim: The aim of this study was to detect genotype HPeV in faecal samples of children and analysis of the clinical symptoms. Method: For the detection and genotyping of HPeV strains, reverse transcription–polymerase chain reaction and sequencing methods were used from faecal samples of children with gastroenteritis divided into three groups: group A) hospitalised children younger than 10 years (n = 75); group B) 0–12 months infants (n = 237) and group C) children less than 18 years of age with sepsis-like/neurological symptoms (n = 105) were tested. Results: Three HPeV positive samples (3/75, 4%) were found in group A, two of them belong to the HPeV type 1, the third was non-typeable. All positive samples were from infants of 7 to 11 months of age. In group B, HPeV was detected in 6.8% (16/237) of the samples. Five were HPeV1, six were HPeV3 and five were non-typeable. While most of the infants with HPeV1 (4/5) did not require hospitalisation, 83% of the HPeV3 infected infants (5/6) did. Five (4.8%) HPeV strains detected from children less than 18 years of age with sepsis-like/neurological symptoms (group C) belonged to HPeV1 (three) and HPeV3 (two). All positive samples were from hospitalised infants less than 2 months of age. Conclusion: HPeV1 infections are less severe in infants than HPeV3 infections. The leading symptom of HPeV1 was diarrhoea, although in infants less than 1–2 months neurological symptoms (somnolence, lassitude) were also present. HPeV3 infections were more common among newborns. The main symptoms of severe HPeV3 infection are: gastroenteritis (7/8), fever ≥38 °C (6/7), loss of appetite (6/7), rash (4/7), somnolence/lassitude (3/7), sepsis-like syndrome (3/7) and respiratory symptoms (2/7). Orv Hetil. 2019; 160(10): 386–395.

JC virus excreted by multiple sclerosis patients and paired controls from Hungary

1998 ◽  
Vol 4 (2) ◽  
pp. 45-48 ◽  
Author(s):  
Gerald L. Stoner ◽  
Hansjürgen T. Agostini ◽  
Caroline F. Ryschkewitsch ◽  
Samuel Komoly
Keyword(s):  
Demyelinating Disease ◽  
Clinical Course ◽  
Jc Virus ◽  
Human Polyomavirus ◽  
European Origin ◽  
The Usa ◽  
Multiple Sclerosis Patients ◽  
Type 3

JC virus (JCV), a human polyomavirus, is the agent of the demyelinating disease progressive multifocal leukoencephalopathy (PML). JCV exists in four main genotypes in the USA. Type 1, including subtypes Type 1A and Type 1B, makes up about 64% of strains in the USA and is thought to be of European origin. Type 2 is found in Asia, and Type 3 in Africa. A fourth type is found only in the USA. In general, these genotypes differ in 1-2.5% of their DNA sequence. Thirty MS patients and 30 paired controls from Budapest were studied. The clinical course of MS was mainly secondary progressive, and patients were stable at the time of testing. Most of the controls were relatives of the probands: a spouse, parent, or child. Overall, 25 of 60 (42%) of the urines tested positive for JCV by PCR. These included 13 of 30 MS patients, and 12 of 30 controls. Genotyping in the VP1 gene showed all 25 JCV strains to be Type 1. Among the MS patients, seven were Type 1A and six were Type 1B. Among the controls, nine were Type 1A and three were Type 1B. In five pairs of MS patients and controls, both were positive for JCV by PCR. Two of these were husband/wife pairs of which one pair was matched for subtype (both Type 1A), and the other was not. Two of them were mother/daughter pairs, and both were matched for subtype (both Type 1B). These findings demonstrate that JCV Type 1 predominates among Hungarians, and suggest that parent/child pairs can be used to trace JCV transmission within the MS family.

scholarly journals Asosiasi antara mutasi gen p16 dengan tipe histopatologi karsinoma nasofaring

2017 ◽  
Vol 47 (1) ◽  
pp. 51
Author(s):  
Muhtarum Yusuf ◽  
Sabilarrusydi Sabilarrusydi ◽  
Mansur Shidiq Wiyadi
Keyword(s):  
Polymerase Chain Reaction ◽  
Nasopharyngeal Carcinoma ◽  
Chain Reaction ◽  
P16 Gene ◽  
Polymerase Chain ◽  
Low Incidence ◽  
Tumor Growth And Metastasis ◽  
Type 3 ◽  
Spearman Test

Latar belakang: Pertumbuhan tumor dan metastasis penderita karsinoma nasofaring (KNF) yangdiduga karena peran beberapa biomarker molekular, dapat diidentifikasi dari spesimen tumor penderitaKNF. Inaktivasi gen p16 akibat mutasi gen p16 dapat digunakan sebagai indikator prognosis dan strategipemberian terapi yang lebih baik pada penderita KNF.Tujuan: Membuktikan asosiasi antara mutasi genp16 dengan tipe histopatologi KNF.Metode: Bahan biopsi dibagi menjadi 2 bagian untuk pemeriksaanhistopatologi dan polymerase chain reaction (PCR). Tipe histopatologi diketahui dari 21 tumor KNFdengan melakukan pengecatan hematoksilin eosin jaringan secara Meyer, terbagi 3 yaitu WHO tipe 1,tipe 2 dan tipe 3. Mutasi gen p16 diperiksa dari jaringan tumor primer KNF dengan PCR, menggunakanmesin Gene Touch Bioneer, dan sekuensing dengan mesin ABI PRISM 310. Analisis statistik menggunakanuji Spearman.Hasil: Didapati sebanyak 21 penderita KNF sesuai kriteria inklusi dan eksklusi. Diketahuisebanyak 19 penderita KNF (90,48%) mengalami mutasi gen p16 negatif. Sebanyak 2 penderita KNF(9,52%) mengalami mutasi gen p16 positif dengan histopatologi WHO tipe 3. Hasil uji Spearmanmendapatkan nilai p=0,568 dan koefisien korelasi sebesar –0,132. Asosiasi antara mutasi gen p16 dengantipe histopatologi (WHO tipe 1, 2, dan 3) pada penderita KNF didapatkan hasil yang tidak bermakna(p>0,05).Kesimpulan: Tidak terdapat asosiasi antara mutasi gen p16 dengan tipe histopatologi KNF.Hal tersebut mungkin oleh karena insidens mutasi gen p16 yang rendah dan faktor etnis.Kata kunci: Karsinoma nasofaring, mutasi gen p16, tipe histopatologi ABSTRACTBackground: Tumor growth and metastasis in nasopharyngeal carcinoma (NPC) patients whichwere presumed caused by the roles of several molecular biomarkers, could be identified in tumor specimensof NPC patients. P16 gene inactivation that was caused by mutation, can be used as an indicator ofprognosis and as strategy for better therapy in NPC. Purpose: To identify the association between p16 genemutation with type of histopathology NPC. Methods: Biopsy specimens were divided for histopathologyexamination and polymerase chain reaction (PCR). Type of histopathology was obtained from 21 NPCtumors by Meyer’s hematoxillin eosin staining, and divided into three types, WHO type 1, type 2 andtype 3. The mutation of p16 gene were identified with PCR from primary tumor tissues by using Bioneertermal cycler machine, and sequencing was performed by ABI PRISM 310. Spearman test was used forstatistical analysis. Results: We found 21 NPC patients who met the inclusion and exclusion criteria.There were 19 (90.48%) NPC patients which had negative mutation of p16 gene. There were 2 NPCpatients (9.52%) who had positive mutation of p16 gene, with histopathology WHO type 3. Spearmantest results showed P=0.568 with a correlation coefficient –0.132. Association of mutation of p16 genewith histopathology type (WHO type 1, 2, 3) in NPC patients was not significant (P>0.05). Conclusion:There was no association found in our study between mutation of p16 gene and histopathological typeof nasopharyngeal carcinoma. It might be caused by low incidence of gene p16 mutation in NPC, andethnic factor.Keywords: Nasopharyngeal carcinoma, mutation of p16 gene, histopathology type

scholarly journals Puerperal Fever and Neonatal Pleural Empyema and Bacteremia Caused by Group A Streptococcus

1998 ◽  
Vol 9 (3) ◽  
pp. 185-188 ◽  
Author(s):  
Laurance Lequier ◽  
Wendy L Vaudry
Keyword(s):  
Chest Tube ◽  
Genomic Sequence ◽  
Puerperal Fever ◽  
Group A Streptococcus ◽  
Pleural Empyema ◽  
Early Postpartum Period ◽  
Early Postpartum ◽  
Group A ◽  
Polymerase Chain

A term neonate developed early onset of sepsis and pleural empyema with group A streptococcus. Her mother also became septic with group A streptococcus in the early postpartum period. The infant required initial chest tube drainage. After reaccumulation of pleural fluid after removal of the chest tube, a thoracotomy with decortication was performed. The isolates of group A streptococcus were analyzed and found to be identical serotypes of the same bacterium. The serotyping revealed both to be M type 1, T pattern 1. Polymerase chain reaction detected the genomic sequence for streptococcal pyrogenic exotoxin A and B in both isolates. With the increase in invasive streptococcal infections in the community, serious perinatal infections may become more frequent.

Molecular analysis of FVIII gene in severe HA patients of Costa Rica

2010 ◽  
Vol 30 (S 01) ◽  
pp. S150-S152
Author(s):  
G. Jiménez-Cruz ◽  
M. Mendez ◽  
P. Chaverri ◽  
P. Alvarado ◽  
W. Schröder ◽  
...  
Keyword(s):  
Factor Viii ◽  
Coagulation Factor ◽  
Costa Rican ◽  
Factor Viii Gene ◽  
Intron 22 Inversion ◽  
Intron 1 ◽  
Polymerase Chain ◽  
Inversion Analysis

SummaryHaemophilia A (HA) is X-chromosome linked bleeding disorders caused by deficiency of the coagulation factor VIII (FVIII). It is caused by FVIII gene intron 22 inversion (Inv22) in approximately 45% and by intron 1 inversion (Inv1) in 5% of the patients. Both inversions occur as a result of intrachromosomal recombination between homologous regions, in intron 1 or 22 and their extragenic copy located telomeric to the FVIII gene. The aim of this study was to analyze the presence of these mutations in 25 HA Costa Rican families. Patients, methods: We studied 34 HA patients and 110 unrelated obligate members and possible carriers for the presence of Inv22or Inv1. Standard analyses of the factor VIII gene were used incl. Southern blot and long-range polymerase chain reaction for inversion analysis. Results: We found altered Inv22 restriction profiles in 21 patients and 37 carriers. It was found type 1 and type 2 of the inversion of Inv22. During the screening for Inv1 among the HA patient, who were Inv22 negative, we did not found this mutation. Discussion: Our data highlight the importance of the analysis of Inv22 for their association with development of inhibitors in the HA patients and we are continuous searching of Inv1 mutation. This knowledge represents a step for genetic counseling and prevention of the inhibitor development.

Characterisation of Type 2N von Willebrand Disease Using Phenotypic and Molecular Techniques

1996 ◽  
Vol 75 (06) ◽  
pp. 959-964 ◽  
Author(s):  
I M Nesbitt ◽  
A C Goodeve ◽  
A M Guilliatt ◽  
M Makris ◽  
F E Preston ◽  
...  
Keyword(s):  
Direct Sequencing ◽  
Von Willebrand Disease ◽  
Molecular Techniques ◽  
Haemophilia A ◽  
Binding Region ◽  
Gene Encoding ◽  
Covalently Linked ◽  
Von Willebrand ◽  
Willebrand Factor

Summaryvon Willebrand factor (vWF) is a multimeric glycoprotein found in plasma non covalently linked to factor VIII (FVIII). Type 2N von Willebrand disease (vWD) is caused by a mutation in the vWF gene that results in vWF with a normal multimeric pattern, but with reduced binding to FVIII.We have utilised methods for the phenotypic and genotypic detection of type 2N vWD. The binding of FVIII to vWF in 69 patients, 36 with type 1 vWD, 32 with mild haemophilia A and one possible haemophilia A carrier with low FVIII levels was studied. Of these, six were found to have reduced binding (five type 1 vWD, one possible haemophilia A carrier), DNA was extracted from these patients and exons 18-23 of the vWF gene encoding the FVIII binding region of vWF were analysed. After direct sequencing and chemical cleavage mismatch detection, a Thr28Met mutation was detected in two unrelated individuals, one of whom appears to be a compound heterozygote for the mutation and a null allele. No mutations were found in the region of the vWF gene encoding the FVIII binding region of vWF in the other four patients

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